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A Protocol for the Production of KLRG1 Tetramer
07:24

A Protocol for the Production of KLRG1 Tetramer

Published on: January 13, 2010

Cutting edge: lectin-like transcript-1 is a ligand for the inhibitory human NKR-P1A receptor

David B Rosen1, Jayaram Bettadapura, Mohammed Alsharifi

  • 1Department of Microbiology and Immunology, The Cancer Research Institute, and Biomedical Sciences Graduate Program, University of California, San Francisco, CA 94143, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|December 13, 2005
PubMed

Insights

The lectin-like transcript-1 (LLT1) is identified as a functional ligand for the C-type lectin receptor NKR-P1A (CD161). This interaction regulates immune cells like NK cells and T cell subsets, impacting immune responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • C-type lectin receptors (CLRs) play crucial roles in immune regulation.
  • The function of human NKR-P1A (CD161), found on NK and T cells, has been largely unknown.
  • Identifying ligands for CLRs is key to understanding immune cell interactions.

Purpose of the Study:

  • To identify the physiologic ligand for the C-type lectin receptor NKR-P1A (CD161).
  • To elucidate the functional consequences of the NKR-P1A-ligand interaction in immune regulation.

Main Methods:

  • Utilized liposomes containing lectin-like transcript-1 (LLT1) to assess binding to NKR-P1A+ cells.
  • Employed antibody inhibition assays to confirm specificity of binding.
  • Constructed chimeric receptors (CD3zeta-NKR-P1A and CD3zeta-LLT1) in reporter cells to study functional activation.
  • Investigated the impact of LLT1 on NK cell cytotoxicity.

Main Results:

  • Demonstrated that LLT1 is a physiologic ligand for NKR-P1A.
  • Confirmed LLT1-NKR-P1A binding using liposome-based assays and antibody blockade.
  • Showed that LLT1 activates reporter cells expressing NKR-P1A, and NKR-P1A activates cells expressing LLT1.
  • Revealed that LLT1 expressed on target cells can inhibit NK cell cytotoxicity through NKR-P1A engagement.

Conclusions:

  • LLT1 is the physiologic ligand for NKR-P1A (CD161).
  • The LLT1-NKR-P1A interaction modulates immune cell function, including NK cell cytotoxicity.
  • This finding provides new insights into the regulatory roles of CLRs in immunity.

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